Cellular Mechanisms Responsible for the Inotropic Action of Insulin on Failing Human Myocardium

Positive inotropy of insulin was not related to catecholamine release and subsequent stimulation of β-adrenergic receptor, but it may enhance the activity of SR Ca2+-ATPase and trans-sarcolemmal Ca2+ entry, mainly via reverse-mode Na+-Ca2+ exchange and insulin-mediated activation of Na+-H+ exchange. We hypothesize that these changes in [Ca2+]i might be secondary to the activation of reverse-mode Na+-Ca2+ exchange, presumably via elevated intracellular Na+ concentration.